Methamphetamine is definitely more harmful than amphetamine when taken recreationally, but I'd argue you're smart to hold off on judging amphetamine to be neuroprotective or even 'neuro-healthy'. Wikipedia should be edited to note that the neuroprotective effects of amphetamines are very debatable and dependent on the way the definition is used. Whoever wrote the wikipedia article may have been a bit biased.
To the OP, I'm not a doctor. I have a degree in biochemistry and molecular biology and am in the process of getting an MD/DO (officially no difference in accreditation after this week, hooray!). I have been published and spent three years doing research at a state university, but I'm not the genius in my crowd. In fact, I'm about average for a medical student. This means I have some experience but am far from an expert at this stage in the game. You should contact a professional if you are interested in getting the best opinion. If you want to read my shitty research, PM me lol. Most of my skepticism of academia was borne from watching people pursue research for the purposes of funding, which creates all kinds of problems when you bring big pharma into the picture... another time.
What's the ISBN # of that pharm text?
978-1451113143
It's Lippincott's review, my bad. Our teachers wrote the book, which comes with an ironic true story: several of the contributing professors are
horrible lecturers b/c they spend most of their time is spent writing the books. Most of us skipped lecture and read that thing cover to cover... so anyone can do it... and they say you have to go college to get an education. Kudos for having the patience to read biochem papers without someone standing over your shoulder. I never could do that. If you're looking for a great lecture series and have the time, Dr. Najeeb's lectures are a must-watch. You can also drop me an email or even skype it up if it would help you get your hands on some good resources.
So I'm wondering if you know, off hand, which subclasses of adrenergic receptors meth is preferentially selective for in comparison to those amp is selective for (and I'd expect this to vary by stereoisomer too). On the other hand, neither is a strong direct adrenergic agonist, particularly meth, so I wouldn't expect these differences to explain much about how the cardiotoxic effects differ between the two.
ebola
No worries.... I believe meth prefers the alpha-2 receptors. Wikipedia has a pretty good list here. We didn't have time to go over ALL of the subclasses, but you can probably figure out which ones it prefers from your own personal research or anecdotes. stimulation of the adrenergics means you're really pushing your system if you remember what's going on simultaneously in your brain.
http://en.wikipedia.org/wiki/Alpha-2_adrenergic_receptor
^These types of pages are indispensable when looking at drug effects bc we often don't know the mechanism and are trying to figure out what you may experience from new rave drug #123897894. The adrenergics are fascinating, imo, especially when you consider how fast the system 'comes online' when you're in danger.
-Methylated compounds cross the BBB into CNS territory with ease compared to regular amphetamines. I'm gonna geek out and mention you can see why meth is taking over crack town when you look at the drug's proposed MOA. Ties in nicely with what
Seppi has been discussing.
I used
wikipedia to look up the answer to
ebola's question and stumbled into what
Seppi was talking about. I noticed some things that may or may not be relevant and have listed them below.
Seppi and ebola
Amp and Meth keep the DAT channel open and inhibits VMAT. Meth apparently binds to VMAT1 and 2 receptors in different regions (of the receptor) and is an agonist of
all subclasses of alpha-2 adrenergic receptors. Direct and indirect MOAs don't have much to do with intensity of effects. It's all about the receptor's affinity for a substrate, the function of the receptor, and how fast the drug is cleared from site of action. If you take enough amp, you may be able to plug the VMAT2 receptor via competitive inhibition (assuming there is some affinity for VMAT2) or pimp VMAT1 so hard it inhibits with the same intensity. I'm confident the substrate affinity and binding times of DAT are more important and well understood. With either drug you still run the risk of frying your brain if you push too hard.
^
The VMAT1 and 2 differences are probably the focus of most amphetamine toxicity studies, which is to say the literature is concerned with determining if amphetamine does indeed exhibit a lack of deleterious effects at therapeutic doses in the isolated system. I have often forgetten this when researching drugs, only to walk away with a nugget the author didn't intend to implant. Here's an obligatory metaphor:
Meth = you're giving justin bieber the keys to your ferrarri for three days.
amphetamine = giving a good friend's relative the keys to your ferrari for a test ride... the stranger could be a Belieber, but your risk is mitigated because you know him better.
I always start with a peer-edited review article when studying a new illness bc it frames the research paradigm and gives you all the terminology/acronyms up front. Wiki is an acceptable source for drugs that don't get you high, imo, b/c there's less of an impetus for self-delusion.
*Just read you had rewritten the wiki,
Seppi. No offense intended but I stand by it.
Later!
). Regardless, I've enjoyed the exchange.
